- Full (HTML) - Full (PDF) - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

Stephen H. Gavett,¹ Najwa Haykal-Coates,¹ Jerry W. Highfill,¹ Allen D. Ledbetter,¹ Lung Chi Chen,² Mitchell D. Cohen,² Jack R. Harkema,³ James G. Wagner,³ and Daniel L. Costa¹

¹National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA; ²Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, USA; ³Michigan State University, East Lansing, Michigan, USA

Abstract

Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 µm (PM_2.5) ] has detrimental respiratory effects in mice to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM_2.5 were derived from settled dust collected at several locations around Ground Zero on 12 and 13 September 2001. Aspirated samples of WTC PM_2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 µg) . This response was not as great as that caused by 100 µg PM_2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM_2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM_2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM_2.5 that would cause comparable doses in people are high (~ 425 µg/m³ for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM_2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM_2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM_2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM_2.5. Key words: airway hyperresponsiveness, inflammation, neutrophil, nose-only inhalation, oropharyngeal aspiration, risk assessment. Environ Health Perspect 111:981-991 (2003) .